Effect of extracellular matrix elements on angiotensin II-induced calcium release in vascular smooth muscle cells from normotensive and hypertensive rats

The interaction of the vascular smooth muscle cells (VSMCs) with the compon ents of the matrix determines several functions of the cell, such as growth and differentiation. In contrast, an alteration in angiotensin (Ang) II-in duced Ca2+ mechanisms in VSMCs was reported in genetic hypertension. In thi s study, we wished to assess the effect of different components of the extr acellular matrix on the increase of [Ca2+], induced by Ang II in VSMCs from spontaneously hypertensive rats (SHR) compared with those from normotensiv e Wistar-Kyoto rats (WKY). Results demonstrate for the first time that elem ents of the extracellular matrix modulate the Ang II-induced Ca2+ transport mechanisms. This modulation is different in cells from WKY compared with t hose from SHR. Thus, growing cells from SHR on collagen I, collagen IV, fib ronectin, vitronectin, or Matrigel induced a significant decrease in Ang II -induced Ca2+ release from internal stores, whereas in cells from WKY, no e ffect could be observed except for those grown on collagen I, which increas ed Ca2+ release. Fibronectin and vitronectin, however, induced a decrease i n Ang II-induced Ca2+ influx in WKY, whereas no effect could be observed in SHR. Conversely, collagen I and collagen IV induced an increase in this in flux in SHR but not in WKY, whereas Matrigel increased the influx in both s trains. These results suggest a modulation of the Ang II-associated signali ng events by the matrix elements via the focal adhesion points. The underst anding of these synergies should provide insight into issues such as develo pment of hypertrophy of large vessels in hypertension.